Heart tachycardia is an abnormally fast rhythm of the heart caused by abnormal electrical propagation. This can be either caused by surviving strands of tissue following a cardiac infarct or a defect in the electrical conduction system of the heart. This abnormal rhythm affects the pumping function of the heart and if not treated could be life-threatening.
Therapies to control tachycardias mostly consist of the use of an implantable Cardiac Defibrillator (ICD), an anti-arrhythmic drug regimen, or ablative strategies. Though ICDs successfully terminate the Ventricular Tachycardia (VT), they do not eliminate the arrhythmogenic substrate and hence do not prevent future recurrences of VT episodes. Anti-arrhythmic drugs, on the other hand, might reduce the incidences of VT occurrences in some patients but have some significant side effects. Ablative strategies, however, reduce and or prevent VT recurrence by locating and ablating the source of the tachycardia. Catheter ablation of ischemic ventricular tachycardia (VT) can be used as a treatment to reduce the burden of VT and defibrillator shocks and can be lifesaving in the event of an arrhythmic storm [R3.1, R3.2]. In addition, recent literature suggests that when VT ablation is performed successfully, it results in a significant decrease in long-term mortality [R3.22].
To facilitate ablation, cardiac mapping can be used to identify potential sites in the heart for ablation by recording electrical signals at multiple sites in the heart. Mapping can be done by either simultaneously acquiring electrograms at various locations of the heart or using a roving electrode and in both cases using surface ECG as a time reference. Local activation time for all of the electrograms can be used to indicate the path of depolarization [R1.1]. Some conventional cardiac mapping techniques used to identify potential sites for ablation include substrate mapping, activation mapping (or isochrone mapping), and entrainment mapping.
Most conventional mapping approaches require activation mapping during tachycardia (i.e. entrainment mapping) for the mapping to identify the putative source. However, these techniques cannot be used in fast or hemodynamically unstable tachycardias or under conditions when tachycardia cannot be induced on arrival to the cath lab. Instead, a variant of mapping is typically used called pace-mapping where electrical stimulation is applied to the heart and the response is mapped to simulate the VT. This mapping can produce ECG data that appears to be like clinical VT however can be produced from a wide area and not necessarily a site that produces success. In substrate mapping during sinus rhythm, a linear lesion along and transecting the scar is used for substrate modification for prevention of VT. Recently, late potential mapping and ablating all of the late potential for scar homogenization has been used; however these lesion sets are not specific and may result in ablating blind alleys and non-critical regions.